Academic literature on the topic 'Developmental origins of adult disease (DOhad)'
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Journal articles on the topic "Developmental origins of adult disease (DOhad)"
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Gilbert, Jeffrey S., and Mark J. Nijland. "Sex differences in the developmental origins of hypertension and cardiorenal disease." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 6 (December 2008): R1941—R1952. http://dx.doi.org/10.1152/ajpregu.90724.2008.
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The “developmental origins of health and disease” (DOHAD) hypothesis derives from clinical observations, indicating long-term health consequences for persons of low birth weight. There is growing evidence, primarily from animal studies, that supports the idea that processes put in motion during development that contribute to DOHAD do not necessarily reflect as significantly compromised growth and altered birth weight. Throughout the body of work investigating the DOHAD hypothesis, several themes have emerged; the importance of the placenta, the presence of critical periods of vulnerability, the involvement of the kidney in programmed hypertension, the presence of sex differences in the progression and development of adult diseases. Despite compelling findings in recent studies, much remains unclear regarding the impact of biological sex in the progression of human diseases, in general, and in the mechanisms underlying developmentally programmed responses, in particular. Although the contribution of biological sex to DOHAD is increasingly recognized, it also appears that it may exert distinctly different influences during fetal and adult life. The mechanisms by which biological sex contributes to these processes remains nebulous at present; nevertheless, several intriguing mechanistic candidates have been proposed ranging from differences in the amounts of sex hormones (e.g., estrogens, androgens) to recently described sexual dimorphism in the transcriptome of a variety of mammalian tissues. Recognizing the influences of biological sex or sex hormones on DOHAD uniquely situates research in this area to provide significant insights into the development and progression of many diseases, recent examples of which are the subject of this review.
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Rosenfeld, C. S. "Homage to the ‘H’ in developmental origins of health and disease." Journal of Developmental Origins of Health and Disease 8, no. 1 (August 31, 2016): 8–29. http://dx.doi.org/10.1017/s2040174416000465.
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Abundant evidence exists linking maternal and paternal environments from pericopconception through the postnatal period to later risk to offspring diseases. This concept was first articulated by the late Sir David Barker and as such coined the Barker Hypothesis. The term was then mutated to Fetal Origins of Adult Disease and finally broadened to developmental origins of adult health and disease (DOHaD) in recognition that the perinatal environment can shape both health and disease in resulting offspring. Developmental exposure to various factors, including stress, obesity, caloric-rich diets and environmental chemicals can lead to detrimental offspring health outcomes. However, less attention has been paid to date on measures that parents can take to promote the long-term health of their offspring. In essence, have we neglected to consider the ‘H’ in DOHaD? It is the ‘H’ component that should be of primary concern to expecting mothers and fathers and those seeking to have children. While it may not be possible to eliminate exposure to all pernicious factors, prevention/remediation strategies may tip the scale to health rather than disease. By understanding disruptive DOHaD mechanisms, it may also illuminate behavioral modifications that parents can adapt before fertilization and throughout the neonatal period to promote the lifelong health of their male and female offspring. Three possibilities will be explored in the current review: parental exercise, probiotic supplementation and breastfeeding in the case of mothers. The ‘H’ paradigm should be the focus going forward as a healthy start can indeed last a lifetime.
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Intapad, Suttira, Norma B. Ojeda, John Henry Dasinger, and Barbara T. Alexander. "Sex Differences in the Developmental Origins of Cardiovascular Disease." Physiology 29, no. 2 (March 2014): 122–32. http://dx.doi.org/10.1152/physiol.00045.2013.
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The Developmental Origins of Health and Disease (DOHaD) proposes that adverse events during early life program an increased risk for cardiovascular disease. Experimental models provide proof of concept but also indicate that insults during early life program sex differences in adult blood pressure and cardiovascular risk. This review will highlight the potential mechanisms that contribute to the etiology of sex differences in the developmental programming of cardiovascular disease.
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Thompson, Michael D., and Brian J. DeBosch. "Maternal Fructose Diet-Induced Developmental Programming." Nutrients 13, no. 9 (September 20, 2021): 3278. http://dx.doi.org/10.3390/nu13093278.
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Developmental programming of chronic diseases by perinatal exposures/events is the basic tenet of the developmental origins hypothesis of adult disease (DOHaD). With consumption of fructose becoming more common in the diet, the effect of fructose exposure during pregnancy and lactation is of increasing relevance. Human studies have identified a clear effect of fructose consumption on maternal health, but little is known of the direct or indirect effects on offspring. Animal models have been utilized to evaluate this concept and an association between maternal fructose and offspring chronic disease, including hypertension and metabolic syndrome. This review will address the mechanisms of developmental programming by maternal fructose and potential options for intervention.
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Islam, Ariful. "Prenatal PUFA undernutrition and risk of adult psychiatric disorders." Bangladesh Journal of Medical Science 15, no. 3 (November 3, 2016): 313–19. http://dx.doi.org/10.3329/bjms.v15i3.21775.
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The developing fetus requires significant amounts of poly unsaturated fatty acids (PUFAs/ FAs) to maintain its normal cellular growth and integrity. Suboptimal intrauterine conditions, including poor PUFAs nutrition, during critical periods of growth may lead to lifelong changes in the bodys organs and tissues, thus providing a physiological basis for adultonset disease. However, the Developmental Origins of Health and Disease (DOHaD) model provide a structure to assess the effect of early nutrition and growth on long-term health. Epidemiological statistics shows that when pregnant mothers experienced malnutrition or famine (e.g. the Dutch Hunger Winter of 1944-1945 and the Chinese famine of 1959-1961), the risk of developing metabolic and psychiatric disease in their children increased. The theory of DOHaD is well referenced in the understanding of adult metabolic diseases, but less so in the field of psychiatric disorders. As PUFAs play critical roles in brain development, considerable effort has been taken in elucidating their function in the pathogenesis of neuropsychiatric disorders.Bangladesh Journal of Medical Science Vol.15(3) 2016 p.313-319
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Magalhães, Elizabeth, Maria Méio, and Maria Moreira. "Hormonal Biomarkers for Evaluating the Impact of Fetal Growth Restriction on the Development of Chronic Adult Disease." Revista Brasileira de Ginecologia e Obstetrícia / RBGO Gynecology and Obstetrics 41, no. 04 (April 2019): 256–63. http://dx.doi.org/10.1055/s-0039-1683904.
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AbstractThe hypothesis of fetal origins to adult diseases proposes that metabolic chronic disorders, including cardiovascular diseases, diabetes, and hypertension originate in the developmental plasticity due to intrauterine insults. These processes involve an adaptative response by the fetus to changes in the environmental signals, which can promote the reset of hormones and of the metabolism to establish a “thrifty phenotype”. Metabolic alterations during intrauterine growth restriction can modify the fetal programming. The present nonsystematic review intended to summarize historical and current references that indicated that developmental origins of health and disease (DOHaD) occur as a consequence of altered maternal and fetal metabolic pathways. The purpose is to highlight the potential implications of growth factors and adipokines in “developmental programming”, which could interfere in the development by controlling fetal growth patterns. These changes affect the structure and the functional capacity of various organs, including the brain, the kidneys, and the pancreas. These investigations may improve the approach to optimizing antenatal as well as perinatal care aimed to protect newborns against long-term chronic diseases.
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Hsu, Chien-Ning, and You-Lin Tain. "Preventing Developmental Origins of Cardiovascular Disease: Hydrogen Sulfide as a Potential Target?" Antioxidants 10, no. 2 (February 5, 2021): 247. http://dx.doi.org/10.3390/antiox10020247.
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The cardiovascular system can be programmed by a diversity of early-life insults, leading to cardiovascular disease (CVD) in adulthood. This notion is now termed developmental origins of health and disease (DOHaD). Emerging evidence indicates hydrogen sulfide (H2S), a crucial regulator of cardiovascular homeostasis, plays a pathogenetic role in CVD of developmental origins. Conversely, early H2S-based interventions have proved beneficial in preventing adult-onset CVD in animal studies via reversing programming processes by so-called reprogramming. The focus of this review will first summarize the current knowledge on H2S implicated in cardiovascular programming. This will be followed by supporting evidence for the links between H2S signaling and underlying mechanisms of cardiovascular programming, such as oxidative stress, nitric oxide deficiency, dysregulated nutrient-sensing signals, activation of the renin–angiotensin system, and gut microbiota dysbiosis. It will also provide an overview from animal models regarding how H2S-based reprogramming interventions, such as precursors of H2S and H2S donors, may prevent CVD of developmental origins. A better understanding of cardiovascular programming and recent advances in H2S-based interventions might provide the answers to bring down the global burden of CVD.
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Bianco-Miotto, T., J. M. Craig, Y. P. Gasser, S. J. van Dijk, and S. E. Ozanne. "Epigenetics and DOHaD: from basics to birth and beyond." Journal of Developmental Origins of Health and Disease 8, no. 5 (September 11, 2017): 513–19. http://dx.doi.org/10.1017/s2040174417000733.
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Developmental origins of health and disease (DOHaD) is the study of how the early life environment can impact the risk of chronic diseases from childhood to adulthood and the mechanisms involved. Epigenetic modifications such as DNA methylation, histone modifications and non-coding RNAs are involved in mediating how early life environment impacts later health. This review is a summary of the Epigenetics and DOHaD workshop held at the 2016 DOHaD Society of Australia and New Zealand Conference. Our extensive knowledge of how the early life environment impacts later risk for chronic disease would not have been possible without animal models. In this review we highlight some animal model examples that demonstrate how an adverse early life exposure results in epigenetic and gene expression changes that may contribute to increased risk of chronic disease later in life. Type 2 diabetes and cardiovascular disease are chronic diseases with an increasing incidence due to the increased number of children and adults that are obese. Epigenetic changes such as DNA methylation have been shown to be associated with metabolic health measures and potentially predict future metabolic health status. Although more difficult to elucidate in humans, recent studies suggest that DNA methylation may be one of the epigenetic mechanisms that mediates the effects of early life exposures on later life risk of obesity and obesity related diseases. Finally, we discuss the role of the microbiome and how it is a new player in developmental programming and mediating early life exposures on later risk of chronic disease.
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Ernst, Jana, Katharina Gert, Frank Bernhard Kraus, Ulrike Elisabeth Rolle-Kampczyk, Martin Wabitsch, Faramarz Dehghani, and Kristina Schaedlich. "Androstenedione changes steroidogenic activity of SGBS cells." Endocrine Connections 9, no. 7 (July 2020): 587–98. http://dx.doi.org/10.1530/ec-19-0549.
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The rapid increase of obesity during the last decades and its future prospects are alarming. Besides the general discussed causes of obesity, the ‘Developmental Origins of Health and Disease’ (DOHaD) hypothesis received more attention in recent years. This hypothesis postulates an adverse influence during early development that programs the unborn child for metabolic dysfunctions later in life. Childhood obesity – an as much increasing problem – can be predisposed by maternal overweight and diabetes. Both, obesity and hyperinsulinemia are major causes of female hyperandrogenemia. As predicted by the DOHaD hypothesis and shown in animal models, developmental androgen excess can lead to metabolic abnormalities in offspring. In this study, we investigated, if androgen exposure adversely affects the adipogenic differentiation of preadipocytes and the endocrine function of adult adipocytes. The human SGBS preadipocyte model was used to affirm the de novo biosynthesis of steroid hormones under normal adipogenesis conditions. Normal adipogenesis was paralleled by an increase of corticosteroids and androgens, whereas estrogen remained at a steady level. Treatment with androstenedione had no effect on SGBS proliferation and differentiation, but adult adipocytes exhibited a significant higher accumulation of triglycerides. Progesterone (up to 2-fold), testosterone (up to 38-fold) and cortisone (up to 1.4-fold) – but not cortisol – were elevated by androstenedione administration in adult adipocytes. Estrogen was not altered. Data suggest that androgen does not negatively influence adipogenic differentiation, but steroidogenic function of SGBS adipocytes.
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Dumesic, Daniel A., Luis R. Hoyos, Gregorio D. Chazenbalk, Rajanigandha Naik, Vasantha Padmanabhan, and David H. Abbott. "Mechanisms of intergenerational transmission of polycystic ovary syndrome." Reproduction 159, no. 1 (January 2020): R1—R13. http://dx.doi.org/10.1530/rep-19-0197.
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Developmental origins of adult disease (DoHAD) refers to critical gestational ages during human fetal development and beyond when the endocrine metabolic status of the mother can permanently program the physiology and/or morphology of the fetus, modifying its susceptibility to disease after birth. The aim of this review is to address how DoHAD plays an important role in the phenotypic expression of polycystic ovary syndrome (PCOS), the most common endocrinopathy of women characterized by hyperandrogenism, oligo-anovulation and polycystic ovarian morphology. Clinical studies of PCOS women are integrated with findings from relevant animal models to show how intergenerational transmission of these central components of PCOS are programmed through an altered maternal endocrine–metabolic environment that adversely affects the female fetus and long-term offspring health. Prenatal testosterone treatment in monkeys and sheep have been particularly crucial in our understanding of developmental programming of PCOS because organ system differentiation in these species, as in humans, occurs during fetal life. These animal models, along with altricial rodents, produce permanent PCOS-like phenotypes variably characterized by LH hypersecretion from reduced steroid-negative feedback, hyperandrogenism, ovulatory dysfunction, increased adiposity, impaired glucose-insulin homeostasis and other metabolic abnormalities. The review concludes that DoHAD underlies the phenotypic expression of PCOS through an altered maternal endocrine–metabolic environment that can induce epigenetic modifications of fetal genetic susceptibility to PCOS after birth. It calls for improved maternal endocrine–metabolic health of PCOS women to lower their risks of pregnancy-related complications and to potentially reduce intergenerational susceptibility to PCOS and its metabolic derangements in offspring.
Dissertations / Theses on the topic "Developmental origins of adult disease (DOhad)"
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Portella, André Krumel. "Investigação sobre o comportamento alimentar na vida adulta de ratos submetidos a regime de superalimentação no período de lactação." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2010. http://hdl.handle.net/10183/29039.
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Alimentação hedônica e homeostática são fatores independentes envolvidos no desenvolvimento da obesidade. Apesar de já se saber que a superalimentação precoce altera a alimentação não hedônica na vida adulta, pouco se sabe sobre seu impacto sobre a preferência por alimentos doces. O objetivo deste trabalho foi o de verificar o comportamento alimentar de ratos superalimentados no período de lactação, com foco principalmente no comportamento alimentar hedônico, e correlacionar com o funcionamento do sistema dopaminérgico mesolímbico, que sabidamente está envolvido na sua regulação. Ninhadas de ratos foram reduzidas a 4 filhotes (ninhada pequena - SL) ou 8 filhotes (ninhada normal - NL) no dia 1 de vida. O desmame ocorreu no dia 21, e todos os testes foram realizados a partir do dia 84 de vida. O consumo de ração foi realizado em condições basais, em resposta à jejum de 24h, na presença de comida palatável (doce), durante isolamento social, e em resposta ao teste de pinçamento da cauda (tail-pinch). Antes de testados com alimento doce, os ratos foram habituados a esse alimento. Locomoção foi aferida em um aparato automatizado. A Área Tegmentar Ventral (VTA) e o Núcleo Accumbens (Acc) foram dissecados a partir de microfatias congeladas. Tecido muscular foi dissecado e processado para medida da fosforilação de AKT (p-AKT) em resposta à insulina. AKT, p-AKT e Tirosina Hidroxilase (TH) foram medidas por método de western-blot. A quantidade de gordura abdominal foi cuidadosamente dissecada e pesada. Resultados: Ratos SL foram mais pesados que os NL em todas as medidas, e ao sacrifício apresentavam maior gordura abdominal (p=0,035). A atividade locomotora não foi diferente quanto à distância percorrida, mas os ratos SL exploraram a região central por mais tempo, indicando menor comportamento ansioso (p=0,036). Não se encontrou diferenças quanto ao consumo de ração padrão (p=0.085) ou alimento doce em condições basais (p=0,65), mas ratos SL tiveram maior consumo de doce num paradigma de escolha com ração-padrão (p=0,017) e em resposta ao estresse de pinçamento da cauda (interação teste x grupo, p=0,006). TH encontrou-se aumentada em ratos SL, tanto no VTA (p=0.016) quanto no Acc (p=0,022). Ratos SL não diferiram quanto a fosforilação do AKT no músculo, porém tiveram menor AKT (p=0,047), o que sugere uma resistência periférica à insulina latente. Em conclusão, a exposição a superalimentação no período de lactação reduz a ansiedade, induz obesidade e programa o comportamento alimentar persistentemente, de maneira que esses animais têm maior preferência por alimento doce. A esses resultados se soma a alteração dos níveis de TH nas vias mesolímbicas, o que sugere a participação destas nessa alteração de comportamento.Hedonic and homeostatic food intakes are independent factors involved in the development of obesity. Although it is well known that early life overfeeding increases food intake in adulthood, little is know about its impact on the palatable food preference in adulthood. We aimed at verifying feeding behavior in this model, with special focus in the hedonic compound, and correlate it to the dopaminergic mesolimbic pathway known to be involved in its regulation. Rat litters were standardized to 4 (small litter - SL) or 8 pups (normal litter- NL) at postnatal day 1. Weaning was at day 21, and all tests were conducted after day 84 of life. Chow consumption was measured at baseline, in response to 24h fasting, in the presence of palatable food, during social isolation and after 1 min. tail pinch stress. Prior to testing sweet food, rats were habituated to the sweet pellets. Locomotion was assessed in an automated box. The ventral tegmentar area (VTA) and nucleus accumbens were micro dissected from frozen brain slices. Muscular tissue was also dissected for assessing the phosphorylation of Akt in response to an insulin challenge. Akt, pAkt and TH proteins were assessed by Western-blot. The abdominal fat content was weighed. Results: SL rats were heavier than NL at all time points and had increased abdominal fat at sacrifice (p=0.035). Locomotor activity was not different with regard to total distance, but RL rats spent more time in the center of the box, an indicative of less anxiety (p=0.036). No difference was found in chow (p=0.085) or sweet food intake at baseline (p=0.65), but SL rats had higher intake of sweet pellets in a two food choice paradigm (p=0.017) and in response to tail pinch stress (test x group interaction, p=0.006). TH was higher in SL rats VTA (p=0.016) and in the nucleus accumbens (p=0.022). SL animals had decreased Akt in the muscle (p=0.047), which suggest a latent peripheral insulin resistance, but p-AKT and the AKT/p-AKT ratio were not different. In conclusion, exposure to overfeeding during the neonatal period decreases anxiety, induces obesity and programs the feeding behavior persistently, in such a way that the animals eat more palatable food. These results are associated with a higher TH protein content and transport in these animals, which suggests that the dopaminergic mesolimbic circuitry may involved in the behavioral findings.
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Picone, Olivier. "Influence de l’alimentation hyperlipidique hypercholestérolémique sur l’expression génique embryonnaire et le développement de maladies à long terme : etudes sur le modèle lapin." Thesis, Paris 11, 2011. http://www.theses.fr/2011PA11T025/document.
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Les problèmes de santé liés à l’alimentation hyperlipidique chez l’humain sont en constante progression. Or, une perturbation de l’environnement fœtal induit chez la descendance une susceptibilité plus grande à développer des maladies à l’âge adulte (DOHad : Developmental Origins of Health and Disease). L’objectif de ce travail de Thèse est d’évaluer, chez le lapin, les conséquences d’une alimentation hypercholestérolémique et hyperlipidique sur le développement embryonnaire, fœtal, et la survenue de troubles métaboliques à long terme.Nous avons nourri des lapines ad libitum avec un régime hypercholéstérolémique (0,2%) et hyperlipidique (8%) (HH) ou un régime témoin (C) à partir de l'âge de 10 (expérience 1) ou de 18 semaines (age de la mise à la reproduction, expérience 2). A la naissance, les portées ont été équilibrées et des croisements effectués pour différencier l'effet de l'alimentation de la mère pendant la gestation et pendant la lactation. Ainsi des lapereaux nés de mères HH ont été allaités par des mères C (groupe HH-C) ou HH (groupe HH-HH) et des lapereaux nés de mère C ont été allaités par des mères C (groupe C-C) ou HH (groupe C-HH). Au cours de l’expérience 1, un retard de croissance intra utérin (RCIU) significatif a été mis en évidence dès 9 jours de gestation par échographie dans le groupe HH (P<0,05). A la naissance, les laperaux étaient significativement plus légers (P<0,05). En raison d’un rattrapage pondéral rapide, il n’existait plus de différence significative au sevrage. Tous les lapins ont alors reçu un aliment témoin distribué ad libitum. A J176, il n’y avait pas de différence de poids entre les groupes HH-HH et HH-C, mais les animaux de ces deux groupes étaient significativement plus lourds que les groupes C-C and C-HH (P<0.05). De plus, la tension artérielle était plus élevée dans le groupe HH-HH par rapport à tous les autres groupes (P<0.05). Au cours de l’expérience 2, de tels effets physiologiques n’ont pas été observés. Les effets physiologiques n'ayant été observés que lorsque le régime avait été commencé avant la gestation, nous avons émis l'hypothèse que l'environnement maternel précoce avait été modifié, entrainant une perturbation du développement embryonnaire à l'origine des conséquences à long terme. l’expression des gènes au moment de la mise en route du génome embryonnaire a été étudié à l’aide d’une puce dédiée. L’analyse transcriptomique a permis de suggérer que certains transcrits étaient présents en quantités différentes. Nous avons montré par qRT-PCR que le régime HH induit une augmentation transitoire de la quantité de transcrit de l’adipophiline (présente à J2 mais pas à J5,5). L’analyse immunohistochimique montre une quantité plus importante de gouttelettes lipidiques localisées près du noyau dans les embryons issus de mères nourries par le régime HH à J5,5 comparé aux témoins. Ces résultats illustrent l’importance de la nutrition avant et pendant la gestation pour la determination de la croissance in utero et postnatale, ainsi que pour le développement de maladies métaboliques à long terme. La nutrition maternelle avant la gestation peut engendrer des modifications d’expression de gènes au moment de la transmission materno embryonnaireThe prevalence of human health problems associated with high-fat diets continues to rise, as does the number of such problems known to be associated with this diet. Disruption of the fetal environment induces in progeny a greater susceptibility to developing diseases in adulthood (DOHad: Developmental Origins of Health and Disease). The objective of the work for this thesis was to assess in rabbits the consequences of a high-cholesterol and high-fat diet on embryonic and fetal development and on the onset of metabolic disorders in the long term.We fed rabbits ad libitum with a high-cholesterol (0.2%) and high-fat (8%) (HH) diet or a control (C) diet, starting at the age of 10 (experiment 1) or 18 weeks (age at which reproduction began, experiment 2).The litters were balanced at birth, and crossings were performed to differentiate the effect of the mother's food during gestation and during lactation. Accordingly, rabbits born to HH mothers were nursed by C (HH-C group) or HH (HH-HH) mothers and those born to C mothers were nursed either by C (C-C) or HH (C-HH) mothers. During experiment 1, ultrasound clearly showed significant intrauterine growth restriction (IUGR) beginning at 9 days of gestation in the HH group (P<0.05). At birth, these rabbits weighed significantly less than their C counterparts (P<0.05). Because of their rapid weight catch-up, the significant difference had disappeared at weaning. All the rabbits thereafter received control food distributed ad libitum. At D176, there was no difference in weight between the HH-HH and HH-C groups but the animals in both these groups were significantly heavier than those in the C-C and C-HH groups (P<0.05). Moreover, blood pressure was higher in the HH-HH group than in any of the other groups (P<0.05). These physiological effects were not observed during experiment 2. Because the physiological effects were observed only when the diet began before gestation, we hypothesized that the early maternal environment been modified, a change that resulted in disruption of embryo development with long-term consequences. We then used a specially designed chip to study gene expression at the maternal to embryonic transition. Transcriptomic analysis suggested that some transcripts were present in different quantities. We showed with qRT-PCR that the HH diet induced a transient augmentation in the quantity of adipophilin transcripts (present at D2 but not at D5.5). The immunohistochemical analysis on D5.5 showed a higher quantity of lipid droplets localized near the nucleus of embryos from mothers fed with the HH diet than in embryos of control mothers. These results illustrate the importance of nutrition before and during pregnancy in the determination of in utero and postnatal growth as well as in the development of metabolic diseases over the long term. Maternal nutrition before conception can engender modifications in gene expression at the moment of the maternal to embryonic transition
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Leveille, Pauline Clémence Elisa. "Etude du lien entre infertilité, obésité et stress oxydant à partir d'un modèle animal et d'une étude cas-témoins chez l'Homme." Thesis, Paris 13, 2013. http://www.theses.fr/2013PA132056.
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L'infertilité affecte près d'un couple sur 6 en France. L’obésité et l'excès de réserves adipeuses, à l'origine de stress oxydant, sont associés à l'infertilité idiopathique. L’équilibre des concentrations entre les pro et antioxydants est assuré par des enzymes antioxydantes, dont la fonction est partiellement contrôlée par des polymorphismes génétiques. De plus, l'altération des gamètes par le stress oxydant pourrait aussi entraîner des conséquences sur le développement d'infertilité chez la descendance. L'objectif de cette étude était d’évaluer les relations entre l’alimentation, le stress oxydant et l’infertilité à travers une étude cas-témoins chez l’Homme et à l’aide d’un modèle animal. Chez l’Homme, le polymorphisme des enzymes impliquées dans le stress oxydant a été étudié chez 110 individus infertiles et 69 fertiles. Le risque d’infertilité est augmenté chez les hommes porteurs d’au moins un allèle Ala-SOD2 (rs4880) et chez les porteurs, hommes et femmes confondus, de deux allèles G-NOS3 (rs1799983). La prise en compte de ces polymorphismes pourrait permettre d’adapter l’alimentation et/ou la prise d’antioxydants selon le génotype du couple infertile idiopathique. Chez la lapine, une alimentation hyperlipidique administrée dès la période prépubertaire a un impact délétère sur la folliculogénèse avec une réduction du nombre de follicules tertiaires et une atrésie folliculaire augmentée par rapport aux témoins. La fonction de l’axe hypothalamo-hypophysaire est aussi perturbée. Chez les descendantes, on observe une atrésie folliculaire augmentée. Ces résultats indiquent qu'une alimentation déséquilibrée en lipides entraine des dysfonctions de l’axe hypothalamo-hypophyso-gonadique chez la mère et ses fillesInfertility affects one in 6 couples. Obesity and excess fat, which induce oxidative stress, have been associated with idiopathic infertility. The balance between pro- and antioxidant enzymes is insured by antioxidant enzymes, which activity partly depends on genetic polymorphisms. Moreover, the alteration of gamete quality through oxidative stress may also affect offspring development and fertility. The aim of the project was to evaluate the association between nutrition, oxidative stress and infertility through a case-control study in humans and using a rabbit model. In humans, the genetic polymorphism of enzymes involved in oxidative stress was studied in 110 infertile and 69 fertile individuals. The presence of at least one Ala-SOD2 allele in men and the presence of two G-NOS3 alleles in both men and women increased the risk of infertility. The analysis of these gene polymorphisms in infertile couples may help adapting nutrition and/or antioxidant intake depending on the couple's genotype. Feeding a hyperlipidic diet to female rabbits from the prepubertal period has a detrimental impact on folliculogenesis, with a reduction in tertiary follicles and an increase in atretic follicles numbers in the ovary, together with an alteration of the hypothalamo-pituitary axis. An increased number of atretic follicles was also observed in adult female offspring. Those results highlight the importance of a high fat diet on hypothalamo-pituitary-gonadal function in females and their offspring
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Cunha, Fábio da Silva. "Similaridades nas desigualdades : um modelo animal para o estudo de vulnerabilidade ao sedentarismo." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2013. http://hdl.handle.net/10183/70421.
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Introdução: O modelo teórico, no qual perfis extremos de desigualdade coexistem num cenário complexo promovendo desfechos de saúde similares, denominado “similaridades nas desigualdades”, surgiu de evidências em humanos. O objetivo deste trabalho foi propor um modelo animal para refletir o fenômeno "similaridades nas desigualdades". Métodos: As ratas prenhes foram randomizadas pelo peso corporal, mantidas individualmente e no dia 10 de gestação foram divididas em três grupos: Controle (Cont), que recebeu ração padrão à vontade; Restrição Alimentar 50% (R50%), que recebeu 50% do consumo do grupo controle e Dieta Rica em Gordura (RG), que recebeu uma dieta rica em gordura à vontade. Essas dietas foram oferecidas a partir do dia 10 de gestação até o dia 21 de lactação. Em até 24 horas após o nascimento, todos os filhotes foram adotados por outras mães, formando os seguintes grupos: Cont_Cont, R50%_Cont, R50%_R50%, Cont_R50%, RG_Cont, RG_RG, Cont_RG. Peso corporal e consumo alimentar das genitoras, peso ao nascer, peso ao longo da vida e exercício físico voluntário foram comparados entre grupos por Equação de Estimação Generalizada (GEE), usando diferentes modelos estatísticos. ANOVA de duas vias foi usada para avaliar os desfechos de gordura abdominal e medidas bioquímicas. Resultados: O peso corporal das genitoras Cont e RG foi maior, comparado ao peso das genitoras R50%. Além de alguns efeitos isolados da exposição às dietas R50% ou RG durante momentos específicos perinatais (gestação e/ou lactação), o efeito das "similaridades nas desigualdades" foi observado no peso ao nascer (ambos filhotes R50% e RG foram mais leves do que os Cont) e na atividade física (os grupos extremos R50%_Cont e RG_Cont foram igualmente diferentes do grupo de referência Cont_Cont, sendo machos menos ativos e fêmeas mais ativas). O acompanhamento do peso corporal ao longo da vida mostrou que os machos pesaram mais que as fêmeas. Nenhum dos três modelos estatísticos evidenciou diferenças entre grupos no total de gordura abdominal. Conclusão: Este estudo contribui com a idéia de que as desigualdades em saúde estão relacionadas a resultados similares em saúde para ambos os extremos populacionais, e propõe um modelo animal para explorar ainda mais este efeito.Introduction: We have previously proposed a theoretical model in which extreme unequal social backgrounds coexist in a complex scenario promoting similar health outcomes, named “Similarities in the inequalities”, and had evidence of this effect in humans. Our objective was to propose an animal model to reflect the “Similarities in the inequalities” phenomenon. Methods: Rats were time-mated and randomly allocated to: Control (Adlib), receiving an ad libitum diet of standard laboratory chow, 50% food restricted (FR), receiving 50% of the ad libitum-fed dam’s intake and high fat diet (HF), receiving a diet containing 45.0% fat. These diets were provided from day 10 of pregnancy throughout the 21-day of lactation. Within 24 hours after birth, all pups were cross-fostered to other dams, forming the following groups: Adlib_Adlib, FR_Adlib, FR_FR, Adlib_FR, HF_Adlib, HF_HF, Adlib_HF. Dam’s body weight and show consumption, pup’s birth weight, growth and physical activity in running wheels, was compared between groups through GEE, using different statistical models. Twoway ANOVA was used to evaluate abdominal fat and biochemical outcomes. Results: Body weight of Adlib and HF dams was higher compared to FR dams. Apart from some isolated effects of the exposure to the FR or HF diets during specific perinatal times (gestation and/or lactation), the “Similarities in the inequalities” effect was seen in birth weight (both FR and HF pups were smaller than Adlib pups) and physical activity (the extreme groups FR_Adlib and HF_Adlib were similarly different from the reference group Adlib_Adlib, being less active in males and more active in females). Body weight monitoring throughout life showed that males were heavier than females. None of the three statistical models showed differences between groups in total abdominal fat. Conclusion: Our study contributes to the idea that health inequalities are related to similar health outcomes for both populational extremes, and proposes an animal model to further explore this effect.
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Brenseke, Bonnie Margaret. "The Role of Maternal High Fat Diet in the Pathogenesis of Metabolic and Bone Disease in the Adult Offspring." Diss., Virginia Tech, 2013. http://hdl.handle.net/10919/49590.
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Chronic diseases such as osteoporosis, type 2 diabetes, and cardiovascular disease are diseases of long duration, slow progression, and are by far the leading cause of death worldwide. A growing body of evidence links adverse exposures in early development with an increased risk of chronic diseases in adult life. The studies presented in this dissertation sought to exploit this phenomenon to determine the extent to which gestational and lactational exposure to a high fat diet predisposes the offspring to certain diseases in later life and if the eating habits of adult offspring would be able to mitigate or exacerbate these conditions. In the study presented in Chapter III, dams fed an atherogenic high fat diet prior to conception and throughout gestation and lactation experienced excess hepatic lipid accumulation and poor birth outcome as characterized by smaller litter sizes and higher post-delivery mortality. In the offspring, gestational and lactational exposure to such a diet resulted in growth restriction and skeletal aberrations indicative of osteoporosis, despite being fed a standard rodent diet post-weaning. We propose that dietary-induced hyperlipidemia, along with pregnancy-associated factors, resulted in fatty liver and subsequently reduced litter sizes and increased early mortality, and that the skeletal aberrations seen in the mature offspring represent dietary-induced inhibition of osteogenesis in favor of adipogenesis. In the study presented in Chapter IV, early exposure to a high fat diet resulted in central obesity, elevated lipid levels, hyperglycemia, and additional markers used in the diagnosis of the metabolic syndrome. Altering the diets of the mature offspring demonstrated that the eating habits of adulthood have the potential to mitigate or exacerbate certain metabolic parameters established earlier in life. Mechanisms contributing to the observed metabolic aberrations could include developmental plasticity and mismatch, catch-up growth, and altered programming of the appetite regulatory network. Collectively, this research suggests that early exposure to a fat-rich diet can lead to metabolic and skeletal aberrations in the adult offspring and adds support to the developmental origins of health and disease hypothesis by finding that adverse nutritional exposures in early life can play a role in the chronic diseases of adulthood. Ph. D.
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Liang, Chengya. "High Saturated Fat Diet Induces Gestational Diabetes, Perinatal Skeletal Malformation and Adult-Onset Chronic Diseases." Diss., Virginia Tech, 2009. http://hdl.handle.net/10919/26700.
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Adult exposure to high fat diet (HFD) has been linked to increased risk of musculoskeletal, cardiovascular, and metabolic diseases; however, the contribution of gestational HFD to elevated oxidative stress (OS), perinatal cardiovascular, skeletal, and metabolic dysfunction as well as long-term effects on adult offspring are incompletely understood. Pathophysiologic mechanisms linking gestational HFD, OS, and insulin resistance to perinatal development and adult-onset chronic diseases are explored in the present study, and maternal antioxidant (quercetin) is offered as a potential preventive dietary supplement to reduce fetal and maternal sequelae of HFD. Female C57BL/6 mice were fed â cafeteria-styleâ HFD (including 32.1% saturated fat to mimic a typical fast food menu) with or without quercetin for one month prior to conception, and throughout gestation. HFD dams developed gestational diabetes with significantly increased placental OS and vasculopathy. Neonates were smaller at birth than age-matched controls, and surviving offspring developed type 2 diabetes, hypertension and osteoporosis during adulthood, despite having been fed healthy diet throughout their postnatal life. Additional measures of bone using three-dimensionally reconstructed computed tomographic image analysis (microCT) revealed microarchitectural changes of bone at birth, and at 6 and 12 months postnatally. Fetuses from HFD dams displayed diminished bone mineral density (BMD) and disrupted endochondral and intramembranous ossification with significantly shortened distal limb lengths, as compared to offspring of standard rodent chow dams. Skeletal malformation persisted into adulthood despite the fact that both control and HFD offspring were fed conventional rodent chow throughout postnatal life. The offspring gestationally exposed to HFD showed significant decreased femoral BMD at 6 months of age and dysregulation of distal femoral trabecular architecture at 12 months of age, indicating development of osteoporosis. We were able to reduce incidence of placental vasculopathy, fetal maldevelopment and adult-onset type 2 diabetes, hypertension and osteoporosis with concurrent maternal quercetin supplementation during pregnancy. Collectively, these data suggested that maternal HFD increases placental OS
and vascular damage during pregnancy, which are associated with fetal malformation and elevated adult-onset multisystemic chronic diseases. Maternal quercetin supplementation must be further explored as a potential dietary intervention for improved placental integrity, fetal development and lifelong health.Ph. D.
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Kawamura, Makoto. "Undernutrition in utero augments systolic blood pressure and cardiac remodeling in adult mouse offspring : possible involvement of local cardiac angiotensin system in developmental origins of cardiovascular disease." Kyoto University, 2007. http://hdl.handle.net/2433/135675.
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Coolidge, Rhonda. "The Relationship of Childhood Stress to Adult Health and Mortality Among Individuals From Two U.S. Documented Skeletal Collections, Late 19th to Early 20th Centuries." Scholar Commons, 2015. http://scholarcommons.usf.edu/etd/5929.
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Although the association between social inequality and poor adult health is well established, the mechanisms by which inequality is translated into poor adult health are less clear. Increasingly, evidence suggests that many adult health problems and health disparities have their origins in early life; the developmental origins of health and disease (DOHaD) hypothesis provides an explanatory mechanism linking adverse early life conditions with permanent structural or functional changes that increase the risk for disease. This hypothesis is consistent with bioarchaeological research noting reduced lifespan among individuals exhibiting signs of childhood stress.
The principal aim of this dissertation is to contribute a bioarchaeological perspective to health disparities research by investigating how health disparities can be measured and understood in the past. This study focuses on early life conditions as a source of adult health disparity by examining a skeletal sample for the association between childhood stress and adult longevity; the relationship between childhood stress and the presence of adult health conditions; and sex, ancestry, and regional differences in these relationships. The study sampled 830 age-documented, U.S. born African American males and females and Euro-American males from the Terry and the Hamann-Todd anatomical collections, representing socially-marginalized individuals from the late 19th- to early 20th centuries. Enamel hypoplasia, femoral length, and vertebral neural canal diameters represented childhood stress; skeletal fractures, tibial periostosis, and the diseased, missing, and filled tooth index represented adult health. Longevity was modeled with Kaplan-Meier survival curves and adult health relationships were modeled with logistic regression. Additionally, cause of death data from historic health department publications and the study sample morgue records were examined for disparity in the epidemiological transition from infectious to degenerative cause of death.
The study found mixed results for all analyses. There was no reduction in longevity for the presence of enamel hypoplasia, short femoral length, or reduced thoracic neural canal diameter. African American males had statistically significant reduced longevity for small lumbar vertebral neural canal diameters. African American males from the Hamann-Todd Collection and Euro-American males from both collections had significant relationships between vertebral neural canal diameters and adult conditions; these relationships varied among the groups but in most cases demonstrated reduced odds for having the adult condition for individuals with smaller canal diameters. African American females had no differential survival or relationships between variables over the lifecourse. All groups except for the Terry Collection Euro-American males continued to have more infectious disease deaths than degenerative disease deaths. The study results contribute to disparities research by demonstrating that the consequences of childhood stress varied by sex and ancestry and by demonstrating within-population variation in timing of the epidemiological transition. Additionally, the study results support the contention of greater male sensitivity to environmental conditions and contributes evidence supporting the DOHaD hypothesis.
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Johnson, William O. "The growth of Bradford infants." Thesis, Loughborough University, 2010. https://dspace.lboro.ac.uk/2134/6327.
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Infant growth is a key indicator of health and a relevant component of paediatric surveillance. Certain growth characteristics are also associated with greater risk for diseases such as obesity and cardiovascular disease. South Asian populations are known to demonstrate poor infant growth and suffer from a high prevalence of non-communicable disease. Relatively little is known about the growth of Pakistani infants, especially following migration. In the United kingdom (UK), infant growth is routinely monitored to detect poor health, and this process produces a repository of largely unutilised data. In 2009, new growth charts, which include a component of the World Health Organisation (WHO) growth standards, were introduced to routine practice. The adoption of prescriptive standards, which are based on breastfed infants living in an unconstrained environment, will have implications for the assessment of growth. To develop and assess the quality of routine growth monitoring data collected in Bradford, UK, so that it can be used to describe the differences in growth between White British and Pakistani infants in the same city. To investigate the factors that influence this growth. To assess the implications of adopting growth standards for practice. The frequency of routine growth monitoring data that are collected at prescribed age periods was assessed. Test-retest growth data were collected from 192 practitioners, and technical error of measurements were calculated. Data on 2464 (boys 51%, White British 45%) infants were submitted to multilevel modelling analysis to produce sex and ethnic specific weight-for-age, abdominal circumference-for-age, head circumference-for-age, and length-for-age growth curves between birth and nine months. Multivariable linear regression models were used to investigate factors that influence size at birth and at nine months. Growth curves were plotted against the WHO standards and the UK 1990 references, Z-scores were calculated, and the relative risks (RR) of underweight, obesity, and poor infant weight gain using the standards compared to the references were assessed. During each prescribed age period for routine growth monitoring generally only 30% to 35% of measurements were recorded. None of the technical error of measurements were excessively large, and coefficients of reliability ranged from 0.96 to 1.00. Multilevel models explained that Pakistani infants were smaller than White British infants, in the first nine months of life, for weight (-210.3g to -321.7g), abdominal circumference (-1.15cm to -0.39cm), head circumference (-0.59cm), and length (-0.32cm). Compared to the WHO standards, infants demonstrated dissimilar weight growth, but similar head circumference and length growth. The common weight growth pattern was slow growth between birth and two months, followed by rapid growth. Using the standards, infants were significantly less likely to be classified as underweight (RR at birth 0.496; 95% Confidence Interval 0.363 to 0.678) and demonstrating poor weight gain from birth to nine months (0.783; 0.644 to 0.952). Growth monitoring data are not collected at prescribed age periods, but following initial training of practitioners are reliable. Integrating research with practice has developed routine data to research calibre and has established protocols to make data more accessible. Pakistani infants were consistently smaller than White British infants, and, despite efforts, the determinants of this phenomenon have not yet been fully elucidated. Growth in weight of infants in Bradford differs significantly from that represented by the WHO standards, and without adequate training of practitioners infant growth may be incorrectly interpreted.
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Arroyo, Juan Pablo. "Exploring Potential Risk Factors of Fetal Origins of Diabetes| Maternal Stressors during Pregnancy and Birth Outcomes among Women in a Hospital in the Municipality of Caguas, Puerto Rico." Thesis, University of South Florida, 2013. http://pqdtopen.proquest.com/#viewpdf?dispub=1543402.
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Puerto Rico has the highest prevalence of type 2 diabetes, low birth-weight, and the second highest prevalence of preterm-birth in all the U.S. and its non-incorporated territories. These conditions are related. Birth-weight at both ends of the spectrum and preterm-birth are associated with an increased risk for developing type 2 diabetes and immune-inflammatory dysregulations. Maternal psychosocial stressors during pregnancy have also been recognized as potential risk factors for type 2 diabetes, and have been consistently associated with preterm-birth and low birth-weight across populations. Current evidence points toward epigenetic fetal metabolic-programming as the mechanism that underlies the increased risk for the previously mentioned morbidities. However, the particular psychosocial stressors that may contribute to the high prevalence of low birth-weight and preterm-birth in the population of Puerto Rico have not been well studied.
The present study assesses the relationships between particular psychosocial stressors, socioeconomic status, food insecurity, and birth outcomes. The results of this study show that low-risk pregnancy women were more likely to have babies with a higher ponderal index if they were exposed to stressors during gestation months 5, 6, and 7, or if exposed to "relationship stress" at any time during pregnancy. Women exposed to "financial difficulties" at any time during pregnancy were more likely to deliver babies at an earlier gestational age. Differences in birth outcomes between the exposed and non-exposed women were independent of maternal anthropometric measurements, maternal age at birth, number of previous births, and sex of the baby. Significant differences in birth outcomes were found between categories of father's self-identified and identified by others ethnicity, but sample size within categories was small. Although mothers with children at home had higher levels of food insecurity, and the level of food insecurity was correlated with higher levels of stress, no birth outcome measure was associated with food insecurity.
Some results are atypical in comparison with other populations, and therefore these findings may contribute to the understanding of population differences in the relationship between maternal stress during pregnancy and birth outcomes. The relatively small sample size and strict exclusion criteria of this study may limit the generalizability of the findings. Epidemiological similarities between Puerto Rico and other populations, and the possibility of a higher ponderal index increasing the risk for type 2 diabetes in the population of Puerto Rico need to be examined in future research.
Books on the topic "Developmental origins of adult disease (DOhad)"
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Kubota, Takeo, and Hideoki Fukuoka, eds. Developmental Origins of Health and Disease (DOHaD). Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-5526-3.
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Macnab, Andrew J., Abdallah Daar, and Christoff Pauw, eds. Health in Transition: Translating developmental origins of health and disease science to improve future health in Africa. African Sun Media, 2020. http://dx.doi.org/10.18820/9781928357759.
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At STIAS, the ‘Health in Transition’ theme includes a programme to address the epidemic rise in the incidence of non-communicable diseases (NCDs) such as Type 2 diabetes, hypertension, obesity, coronary heart disease and stroke in Africa. The aim is to advance awareness, research capacity and knowledge translation of science related to the Developmental Origins of Health and Disease (DOHaD) as a means of preventing NCDs in future generations. Application of DOHaD science is a promising avenue for prevention, as this field is identifying how health and nutrition from conception through the first 1 000 days of life can dramatically impact a developing individual’s future life course, and specifically predicate whether or not they are programmed in infancy to develop NCDs in later life. Prevention of NCDs is an essential strategy as, if unchecked, the burden of caring for a growing and ageing population with these diseases threatens to consume entire health budgets, as well as negatively impact the quality of life of millions. Africa in particular needs specific, focussed endeavors to realize the maximal preventive potential of DOHaD science, and a means of generating governmental and public awareness about the links between health in infancy and disease in adult life. This volume summarizes the expertise and experience of a leading group of international scientists led by Abdallah Daar brought together at STIAS as part of the ‘Health in Transition’ programme.
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Bhopal, Raj S. Epidemic of Cardiovascular Disease and Diabetes. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198833246.001.0001.
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Coronary heart disease (CHD) and stroke, collectively cardiovascular disease (CVD), are caused by narrowing and blockage of the arteries supplying the heart and brain, respectively. In type 2 diabetes (DM2) insulin is insufficient to maintain normal blood glucose. South Asians have high susceptibility to these diseases. Drawing upon the scientific literature and discussions with 22 internationally recognized scholars, this book focuses on causal explanations and their implications for prevention and research. Genetically based hypotheses are considered together with the developmental origins of health and disease (DOHAD) family of hypotheses. The book then considers how CHD, stroke, and DM2 are closely linked to rising affluence and the accompanying changes in life-expectancy and lifestyles. The established causal factors are shown to be insufficient, though necessary, parts of a convincing explanation for the excess of DM2 and CVD in South Asians. In identifying new explanations, this book emphasizes glycation of tissues, possibly leading to arterial stiffness and microcirculatory damage. In addition to endothelial pathways to atherosclerosis an external (adventitial) one is proposed, i.e. microcirculatory damage to the network of arterioles that nourish the coronary arteries. In addition to the ectopic fat in their liver and pancreas as the cause of beta cell dysfunction leading to DM2, additional ideas are proposed, i.e. microcirculatory damage. The high risk of CVD and DM2 in urbanizing South Asians is not inevitable, innate or genetic, or acquired in early life and programmed in a fixed way. Rather, exposure to risk factors in childhood, adolescence, and most particularly in adulthood is the key. The challenge to produce focused, low cost, effective actions, underpinned by clear, simple, and accurate explanations of the causes of the phenomenon is addressed.
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Ruiz-Villalba, Adrián, Nikolaos Frangogiannis, and José Maria Pérez-Pomares. Origin and diversity of cardiac fibroblasts: developmental substrates of adult cardiac fibrosis. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0012.
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Cardiac connective tissues are primarily formed by cardiac fibroblasts (CF) of diverse embryonic origins. Whereas CF specific roles in cardiac morphogenesis remain under-researched, their involvement in adult cardiac fibrosis is clinically relevant. Cardiac fibrosis is a common element of several chronic cardiac conditions characterized by the loss of ventricular wall mechanical function, ultimately driving to heart failure. In the ischaemic heart early reparative fibrosis evidences the very restricted regenerative potential of the myocardium. In non-ischaemic diseases fibrosis is activated by unknown signals. We summarize current knowledge on the origin of CFs and their developmental roles, and discuss the differential disease-dependent response of different CF subpopulations to various pathological stimuli. We also describe the characteristic cell-cell and cell-matrix interactions that determine the fibrotic remodelling of the myocardium. We analyse experimental models for the study of cardiac fibrosis, and suggest future directions in the search for new markers and therapeutic targets.
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Pérez-Pomares, José M., and Robert Kelly, eds. The ESC Textbook of Cardiovascular Development. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.001.0001.
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A rapid inspection of the table of contents shows that we have grouped relevant cardiovascular developmental topics in five different sections, which move progressively from basic research to clinical relevance, concluding with a glance at the near future of this fast-moving field. All of these sections deal with concepts that are critical to understanding from where and how cardiac chambers (atria and ventricles), valves (atrioventricular and arterial), great vessels (aortic and pulmonary trunks), cardiac conduction system (nodes, bundles, and Purkinje fibres), and coronary blood vessels form. Throughout the book there is continuous reference to experimental animal models for developmental processes, including the mouse, chick, and zebrafish, often involving the application of state of the art technological innovations. This has allowed us to illustrate the more likely origins of specific forms of congenital heart disease, and to elaborate on the developmental substrate of certain forms of adult cardiovascular disease.
Book chapters on the topic "Developmental origins of adult disease (DOhad)"
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Sata, Fumihiro. "Developmental Origins of Health and Disease (DOHaD) Cohorts and Interventions: Status and Perspective." In Current Topics in Environmental Health and Preventive Medicine, 53–70. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-2194-8_4.
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Godfrey, Keith M., Karen A. Lillycrop, Mark A. Hanson, and Graham C. Burdge. "Epigenetic Mechanisms in the Developmental Origins of Adult Disease." In Epigenetic Aspects of Chronic Diseases, 187–204. London: Springer London, 2011. http://dx.doi.org/10.1007/978-1-84882-644-1_13.
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Embleton, Nicholas D., Claire L. Wood, and Robert J. Tinnion. "Catch up Growth and the Developmental Origins of Health and Disease (DOHaD) in Preterm Infants." In Nutrition for the Preterm Neonate, 269–90. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6812-3_14.
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Nicholas, L. M., and S. E. Ozanne. "The Developmental Origins of Health and Disease—Where Did It All Begin?" In Fetal and Early Postnatal Programming and Its Influence on Adult Health, 3–16. Boca Raton : Taylor & Francis, 2017. | Series: Oxidative stress and disease: CRC Press, 2017. http://dx.doi.org/10.1201/9781315154312-1.
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Krechowec, Stefan O., Nichola M. Thompson, and Bernhard H. Breier. "Fetal Growth Restriction and the Developmental Origins of Adult Disease Hypothesis: Experimental Studies and Biological Consequences." In Small for Gestational Age, 26–43. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000165959.
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Bailey, Kathryn A. "Developmental Origins of Adult Disease." In Systems Biology in Toxicology and Environmental Health, 239–53. Elsevier, 2015. http://dx.doi.org/10.1016/b978-0-12-801564-3.00011-0.
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Gluckman, Peter D., Tatjana Buklijas, and Mark A. Hanson. "The Developmental Origins of Health and Disease (DOHaD) Concept." In The Epigenome and Developmental Origins of Health and Disease, 1–15. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-801383-0.00001-3.
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Junien, Claudine, Sara Fneich, Polina Panchenko, Sarah Voisin, and Anne Gabory. "Sexual Dimorphism and DOHaD through the Lens of Epigenetics." In The Epigenome and Developmental Origins of Health and Disease, 389–424. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-801383-0.00020-7.
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Sun, Congshan, Miguel A. Velazquez, and Tom P. Fleming. "DOHaD and the Periconceptional Period, a Critical Window in Time." In The Epigenome and Developmental Origins of Health and Disease, 33–47. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-801383-0.00003-7.
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Devaskar, Sherin U., and Kara Calkins. "Developmental origins of adult health and disease." In Fanaroff and Martin's Neonatal–Perinatal Medicine, 229–42. Elsevier, 2011. http://dx.doi.org/10.1016/b978-0-323-06545-0.00022-4.
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